Inhibition of [<sup>3</sup>H]‐(+)‐MK 801 binding to rat brain sections by CPP and 7‐chlorokynurenic acid: an autoradiographic analysis

Tacconi, Stefano; Ratti, Emiliangelo; Marien, Marc; Gaviraghi, G.; Bowery, Norman G.

doi:10.1111/j.1476-5381.1993.tb12845.x

Cited by 25 publications

(5 citation statements)

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“…Stimulation of the LOT elicited a surface negative waveform which is the result of the release of acidic amino-acid (Collins, 1979) acting on x-amino-3-hydroxy-5-methyl-4isoxazoleproprionic acid (AMPA) type receptors (Collins & Buckley, 1989). NMDA receptors are present in olfactory cortex (Tacconi et al, 1993) and they may also be involved in synaptic transmission (Collins, 1991) but in our experiments, this component did not contribute to the evoked potential (see below). When recordings were made from an area of the slice close to the LOT, the synaptic potential was preceded by a shorter transient response due to the activity of the axons underlying the recording electrode.…”

Section: Resultsmentioning

confidence: 55%

“…NMDA receptors are present in olfactory cortex (Tacconi et al, 1993) and they may also be involved in synaptic transmission (Collins, 1991) Figure 1 but can be seen with both preparations in Figure 2. The fibre potential is close to the stimulus artefact but it can be distinguished by comparing the response labelled 'anoxia' in Figure 2 where all the biologically generated responses had been lost.…”

Section: Resultsmentioning

confidence: 99%

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NMDA antagonists increase recovery of evoked potentials from slices of rat olfactory cortex after anoxia

Yassin

Scholfield

1994

British J Pharmacology

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1 The role of glutamate in producing tissue damage during cerebral anoxia was investigated in brain slices using antagonists to the NMDA and AMPA receptor types. 2 Tissue function was assessed by field recordings of the synaptically evoked potentials elicited by stimulating the main afferent input to the olfactory cortex, the lateral olfactory tract. Anoxia was produced by bathing the slice in glucose-free solution equilibrated with 95% N2/5% CO2. 3 The amount of recovery of the evoked potential was inversely dependent on the period of anoxia and temperature: at 24°C, 15 min of anoxia followed by reoxygenation produced a 14.6 ± 4.1 % recovery whereas there was no recovery at 35°C. 4 Dizocilpine and ketamine had no effect on synaptic transmission in oxygenated media but following anoxia they produced an increased recovery of the responses: from 14.6 ± 4.1 % to 48.3 ± 7.8% for dizocilpine (10 AM) and 21.6 ± 7.7% to 87.2 ± 7.1% for ketamine (200,M)

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Section: Resultsmentioning

confidence: 55%

Section: Resultsmentioning

confidence: 99%

NMDA antagonists increase recovery of evoked potentials from slices of rat olfactory cortex after anoxia

Yassin

Scholfield

1994

British J Pharmacology

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“…The in vitro preparations used to visualize the localisation of NMDArs are likely to contain concentrations of endogenous agonists that are high enough to fully activate the receptors. This is evident from autoradiographic experiments, in which exogenously applied glutamate and glycine do not enhance the binding of [ 3 H]MK-801 to NMDArs above baseline levels [29][30]. Since access to the ion-channel site depends on the concentration of glutamate and glycine [7], the in vitro binding of radioligands to maximally activated receptors may not necessarily reflect their in vivo uptake, and thus correspond to the PET-measurable distribution of NMDArs.…”

Section: Discussionmentioning

confidence: 99%

Preclinical evaluation of [18F]PK-209, a new PET ligand for imaging the ion-channel site of NMDA receptors

Golla

Klein

Bakker

et al. 2015

Nuclear Medicine and Biology

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“…Therefore, we used this same dose in the current studies with ETI and QNP. CPP is a non-competitive NMDA receptor antagonist which possesses good selectivity and a relatively high ( K i for CPP=7.3 μM) dissociation constant (Tacconi et al 1993). In the current study CPP was administered using a dose of 1 mg/kg.…”

Section: Methodsmentioning

confidence: 99%

Impact of dopamine–glutamate interactions on striatal neuronal nitric oxide synthase activity

et al. 2009

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Rationale-It is known that dopamine (DA) D1 receptor activation stimulates striatal nitric oxide (NO) synthesis, whereas D2 receptor activation produces the opposite effect. However, the mechanisms involved in the dopaminergic modulation of NO synthase (NOS) are unknown.Objectives-We hypothesized that the effects of DA on striatal NO signaling are dependent on ongoing glutamatergic activation of NOS. Therefore, the current study examined whether intact NMDA receptor activation is required for the dopaminergic modulation of NOS activity. Methods-We assessed the impact of pharmacological manipulations of D1, D2 and NMDA receptors on NOS activity in the dorsal striatum and motor cortex using nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry. Drugs were administered systemically to conscious animals and NADPH-d staining was quantified in these regions using ex vivo measurements of tissue optical density.Results-Administration of the neuronal NOS inhibitor N G -propyl-L-arginine (NPA), the D1 receptor antagonist SCH 23390, and the NMDA receptor antagonist 3-phosphonopropylpiperazine-2-carboxylic acid (CPP) all attenuated staining selectively in the striatum. Administration of the D2 receptor agonist quinpirole decreased NADPH-d staining in both the striatum and cortex. Striatal NADPH-d staining elicited by administration of the D1 receptor agonist SKF 81297 or the D2 receptor antagonist eticlopride was attenuated by NPA, SCH 23390, and CPP pretreatment. Quinpirole pretreatment also abolished the facilitatory effect of SKF 81297.Conclusions-These studies show for the first time that ongoing NMDA receptor activation is necessary for modulation of striatal NOS activity by both facilitatory (D1 receptor activation) and inhibitory (D2 receptor activation) dopaminergic signaling mechanisms. Keywords dopamine; nitric oxide; nitric oxide synthase; NMDA receptor; striatum; cortex Nitric oxide (NO) is a key modulator of neuronal activity in the dorsal striatum and is thought to play an important role in complex processes including control of motor function and motivated behavior (Prast and Philippu 2001;West et al. 2002;Del Bel et al. 2005). NO is synthesized within medium-sized aspiny interneurons by type-1/neuronal NO synthase (nNOS). Striatal nNOS expressing interneurons and their processes are readily labeled using nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemical staining techniques (Hope et al.

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Inhibition of [³H]‐(+)‐MK 801 binding to rat brain sections by CPP and 7‐chlorokynurenic acid: an autoradiographic analysis

Abstract: The regional binding of [3H]-(+)-5-methyl-10,11-dihydro-5H-dibenzo(a,d)cyclohepten-5,10-imine

Cited by 25 publications

References 32 publications

NMDA antagonists increase recovery of evoked potentials from slices of rat olfactory cortex after anoxia

NMDA antagonists increase recovery of evoked potentials from slices of rat olfactory cortex after anoxia

Preclinical evaluation of [18F]PK-209, a new PET ligand for imaging the ion-channel site of NMDA receptors

Impact of dopamine–glutamate interactions on striatal neuronal nitric oxide synthase activity

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Inhibition of [3H]‐(+)‐MK 801 binding to rat brain sections by CPP and 7‐chlorokynurenic acid: an autoradiographic analysis

Abstract: The regional binding of [3H]-(+)-5-methyl-10,11-dihydro-5H-dibenzo(a,d)cyclohepten-5,10-imine

Cited by 25 publications

References 32 publications

NMDA antagonists increase recovery of evoked potentials from slices of rat olfactory cortex after anoxia

NMDA antagonists increase recovery of evoked potentials from slices of rat olfactory cortex after anoxia

Preclinical evaluation of [18F]PK-209, a new PET ligand for imaging the ion-channel site of NMDA receptors

Impact of dopamine–glutamate interactions on striatal neuronal nitric oxide synthase activity

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Product

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Inhibition of [³H]‐(+)‐MK 801 binding to rat brain sections by CPP and 7‐chlorokynurenic acid: an autoradiographic analysis